| pubmed-article:81682 | pubmed:abstractText | The effects of therapeutic intensities of ultrasound on human platelets in whole blood were investigated by monitoring the release of the platelet specific protein beta-thromboglobulin (beta-TG). More beta-TG was released as the intensity of the ultrasound was increased and also as the driving frequency was decreased from 3.0 to 0.75 MHz. Some beta-TG was released at spatially-averaged intensities as low as 0.6 W/cm2 at 0.75 MHz, a value significantly lower than that observed for the onset of aggregation of platelet rich plasma (obtained from the same volunteer) in the same exposure system. Liberation of beta-TG by ultrasound was diminished but not abolished in the presence of inhibitors which rendered the platelets functionally inert. Our data suggests that beta-TG is liberated in two ways, firstly as a result of platelet disruption by cavitation, and subsequently by potent aggregating agents, liberated in parallel with beta-TG, inducing the physiological release reaction in adjacent platelets. The low therapeutic intensities and short exposure times (30 s or less) necessary to liberate beta-TG from normal human platelets in vitro, suggests that patients with abnormally sensitive platelets and/or 'hypercoagulable state' could be at risk if subjected to high therapeutic intensities of ultrasound. | lld:pubmed |
